{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Sun W"],"funding":["HHS | National Institutes of Health","American Cancer Society","Alex's Lemonade Stand Foundation for Childhood Cancer","NIAID NIH HHS","NCI NIH HHS","NIGMS NIH HHS"],"pagination":["501-514"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8983472"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["20(4)"],"pubmed_abstract":["Growth factor independence-1 (GFI1) is a transcriptional repressor and master regulator of normal and malignant hematopoiesis. Repression by GFI1 is attributable to recruitment of LSD1-containing protein complexes via its SNAG domain. However, the full complement of GFI1 partners in transcriptional control is not known. We show that in T-acute lymphoblastic leukemia (ALL) cells, GFI1 and IKAROS are transcriptional partners that co-occupy regulatory regions of hallmark T-cell development genes. Transcriptional profiling reveals a subset of genes directly transactivated through the GFI1-IKAROS partnership. Among these is NOTCH3, a key factor in T-ALL pathogenesis. Surprisingly, NOTCH3 expression by GFI1 and IKAROS requires the GFI1 SNAG domain but occurs independent of SNAG-LSD1 binding. GFI"],"journal":["Molecular cancer research : MCR"],"pubmed_title":["GFI1 Cooperates with IKZF1/IKAROS to Activate Gene Expression in T-cell Acute Lymphoblastic Leukemia."],"pmcid":["PMC8983472"],"funding_grant_id":["P30 CA042014","R01CA201235","R01AI100873","R01 GM122778","R01 AI100873","R01GM122778","R01 CA201235","P30CA042014"],"pubmed_authors":["Cairns BR","Engel ME","Guo J","Tantin D","Bareyan D","Poeschla A","Sun W","Casey MJ","McClellan D"],"additional_accession":[]},"is_claimable":false,"name":"GFI1 Cooperates with IKZF1/IKAROS to Activate Gene Expression in T-cell Acute Lymphoblastic Leukemia.","description":"Growth factor independence-1 (GFI1) is a transcriptional repressor and master regulator of normal and malignant hematopoiesis. Repression by GFI1 is attributable to recruitment of LSD1-containing protein complexes via its SNAG domain. However, the full complement of GFI1 partners in transcriptional control is not known. We show that in T-acute lymphoblastic leukemia (ALL) cells, GFI1 and IKAROS are transcriptional partners that co-occupy regulatory regions of hallmark T-cell development genes. Transcriptional profiling reveals a subset of genes directly transactivated through the GFI1-IKAROS partnership. Among these is NOTCH3, a key factor in T-ALL pathogenesis. Surprisingly, NOTCH3 expression by GFI1 and IKAROS requires the GFI1 SNAG domain but occurs independent of SNAG-LSD1 binding. GFI","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Apr","modification":"2026-06-01T02:23:22.409Z","creation":"2025-04-05T20:47:40.604Z"},"accession":"S-EPMC8983472","cross_references":{"pubmed":["34980595"],"doi":["10.1158/1541-7786.MCR-21-0352","10.1158/1541-7786.mcr-21-0352"]}}